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  • Rockefeller University Press  (7)
  • 1985-1989  (7)
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  • Rockefeller University Press  (7)
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  • 1985-1989  (7)
Year
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Sequence analysis and expression of an X-linked, lymphocyte-regulated gene family (XLR).
    Rockefeller University Press ; 1987
    In:  The Journal of experimental medicine Vol. 166, No. 6 ( 1987-12-01), p. 1702-1715
    Details
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 166, No. 6 ( 1987-12-01), p. 1702-1715
    Abstract: The XLR gene family consists of approximately 10 X-linked genes, the expression of which is regulated in lymphocyte development. Certain members of the gene family are closely linked to the murine xid immune deficiency mutation. Sequence analysis of a cDNA clone pM1 derived from the plasmacytoma MOPC167 showed an open reading frame capable of coding for a protein of 208 amino acids and mol wt 24,000. The lack of a signal peptide or transmembrane region indicates a probable cytoplasmic or nuclear localization for the predicted pM1 protein. The predicted protein shares significant homology with lamins A and C and other members of the intermediate filament family of proteins, and shares features important for the coiled-coil structure proposed for these proteins. Analysis of cDNA clones derived from a presecretory lymphoma and from adult thymus indicates that B and T lymphocytes transcribe a common major mRNA identical to pM1, while other rare transcripts were also identified by these studies. A series of clonal T lymphoma lines representing distinct stages of thymic differentiation showed that, as with B lymphoid tumors, XLR expression is correlated with the maturation of the thymomas.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.166.6.1702
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1987
    detail.hit.zdb_id: 1477240-1
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    Online Resource
  • 2
    Online Resource
    Online Resource
    C-reactive protein mediates the solubilization of nuclear DNA by complement in vitro.
    Rockefeller University Press ; 1985
    In:  The Journal of experimental medicine Vol. 161, No. 6 ( 1985-06-01), p. 1344-1356
    Details
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 161, No. 6 ( 1985-06-01), p. 1344-1356
    Abstract: We have studied the interaction of C-reactive protein (CRP)-chromatin complexes with serum. The amount of chromatin solubilized by serum is directly proportional to the amount of CRP present. Serum minus C3 did not appreciably solubilize chromatin within the time allowed in these experiments regardless of the amount of CRP present. This indicates that, in addition to CRP, complement is critical to the solubilization process. Studies using genetically C2-deficient serum and purified C2 indicate that the classical complement pathway is primarily involved in the solubilization, however, there may be minor involvement by the alternative pathway. We used an enzyme-linked immunosorbent assay to determine the amounts of CRP in plasma from eight patients with systemic lupus erythematosus; two of the eight had levels of CRP far lower than previously reported for normal individuals, and an additional sample had antibodies reactive with CRP. Together, these results suggest that one of the functions of CRP is to mediate the removal of exposed nuclear DNA by complement-dependent solubilization of chromatin. A defect in this mechanism could (a) facilitate the production of antibodies against chromatin components exposed due to tissue damage or (b) contribute to immune complexes containing the chromatin components released from damaged tissue because they are not rapidly cleared.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.161.6.1344
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1985
    detail.hit.zdb_id: 1477240-1
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Oncogene expression in autoimmune and normal peripheral blood mononuclear cells.
    Rockefeller University Press ; 1986
    In:  The Journal of experimental medicine Vol. 163, No. 5 ( 1986-05-01), p. 1292-1307
    Details
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 163, No. 5 ( 1986-05-01), p. 1292-1307
    Abstract: PBMC from patients with autoimmune diseases and from normal controls were studied for the expression of several cellular oncogenes. Gene expression was assessed by Northern blot analysis of poly(A)+ RNA obtained from leukapheresis samples. Patients with SLE expressed significantly more c-myc protooncogene RNA than did normal controls. Increased expression of the N-ras protooncogene was found in that subset of patients whose autoimmune disease was very active. Cells from individuals with SLE, but not from those with other autoimmune illnesses, showed significantly decreased levels of the c-myb and c-fos protooncogenes. To examine the implications of these findings, B and T cells were purified from apheresis samples donated by normal volunteers. When mitogen was used to activate the B cells in vitro, their pattern of protooncogene expression changed to resemble that found in freshly isolated cells from lupus patients. These results suggest that the differences detected in the expression of protooncogenes by patients with SLE may be due to the abnormal activation of their B cells in vivo. The pattern of protooncogene expression found in patients with other autoimmune illnesses is consistent with the activation of additional cell types in those diseases.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.163.5.1292
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1986
    detail.hit.zdb_id: 1477240-1
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  • 4
    Online Resource
    Online Resource
    Systemic autoimmune disease arises from polyclonal B cell activation.
    Rockefeller University Press ; 1987
    In:  The Journal of experimental medicine Vol. 165, No. 6 ( 1987-06-01), p. 1755-1760
    Details
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 165, No. 6 ( 1987-06-01), p. 1755-1760
    Abstract: The number of B cells producing antibodies reactive with any of seven autoantigens or two conventional antigens was compared at the single-cell level to the total number of Ig-secreting B cells present in the spleens of NZB, MRL lpr/lpr, and BXSB autoimmune mice. The proportion of lymphocytes producing antibodies of each specificity, expressed as a percentage of the total B cell repertoire, was virtually identical among autoimmune and congenic nonautoimmune animals. Furthermore, B cells and serum antibodies reactive with conventional antigens increased commensurately with those reactive with autoantigens. These results indicate that systemic autoimmune diseases arise from polyclonal B cell activation.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.165.6.1755
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1987
    detail.hit.zdb_id: 1477240-1
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  • 5
    Online Resource
    Online Resource
    High hepatic natural killer cell activity in murine lupus.
    Rockefeller University Press ; 1987
    In:  The Journal of experimental medicine Vol. 166, No. 1 ( 1987-07-01), p. 271-276
    Details
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 166, No. 1 ( 1987-07-01), p. 271-276
    Abstract: This study demonstrates a profound elevation of NK activity, as measured by cytotoxicity to YAC-1 targets in a 4-h incubation 51Cr-release assay, of freshly isolated hepatic NPC from both MRL/lpr and (NZB X NZW)F1 mice. This marked increase was not observed in splenic or peripheral blood NK. The hepatic NK were nonadherent, radioresistant, Ly-1-,2-, and AGM1+. Furthermore, biologic response modifiers can further augment hepatic NK activity in these autoimmune strains.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.166.1.271
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1987
    detail.hit.zdb_id: 1477240-1
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  • 6
    Online Resource
    Online Resource
    Clonal expansion of abnormal B cells in old NZB mice.
    Rockefeller University Press ; 1987
    In:  The Journal of experimental medicine Vol. 166, No. 5 ( 1987-11-01), p. 1585-1590
    Details
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 166, No. 5 ( 1987-11-01), p. 1585-1590
    Abstract: The spleens of old NZB mice have an abnormal population of B cells with extra chromosomes. These hyperdiploid B cells manifest increased proliferative capacity; they grow in (NZB X DBA/2)F1 spleens after intravenous injections. Molecular analysis of individual old NZB and F1 passaged spleens demonstrate that hyperdiploid cells represent a clonal or oligoclonal expansion of B cells. All spleens with at least 10% hyperdiploid cells demonstrated both heavy and kappa light chain immunoglobulin gene rearrangements by Southern blot hybridization. None of the hyperdiploid spleens from old NZB mice had lambda rearrangements and only one of five showed evidence of clonal rearrangement of the TCR-beta gene. One also had a VK10 clonal rearrangement. Elevated p53 oncogene protein was observed in NZB hyperdiploid spleen cells; however, no p53 or other oncogene rearrangements or amplifications were seen. Hyperdiploid cells were IgM-bright, IgD-dull, Ia+, dull B220, Thy-1-, and Ly-1-dull. Spleens with hyperdiploid B cells had increased percentages of Ly-1 B cells. The data suggest that hyperdiploid cells in old NZB mice represent clonal expansion of B cells and that they may represent an intermediate stage between autoimmunity and malignancy.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.166.5.1585
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1987
    detail.hit.zdb_id: 1477240-1
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  • 7
    Online Resource
    Online Resource
    Genetic analysis of autoimmune gld mice. I. Identification of a restriction fragment length polymorphism closely linked to the gld mutation within a conserved linkage group.
    Rockefeller University Press ; 1988
    In:  The Journal of experimental medicine Vol. 167, No. 2 ( 1988-02-01), p. 688-693
    Details
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 167, No. 2 ( 1988-02-01), p. 688-693
    Abstract: A linkage map of distal mouse chromosome 1 was generated using restriction fragment length polymorphism (RFLP) analysis of DNA prepared from 95 [C3H-gld/gld X Mus spretus)F1 X C3H-gld/gld] backcross mice. The gene order was: (centromere) C4bp, Ren-1,2, Ly-5, [At-3/gld] , Apoa-2/Ly-17, Spna-1 (telomere). All mice expressing the phenotype of gld homozygotes were homozygous for the At-3 RFLP characteristic of C3H mice and none of the mice heterozygous for At-3 RFLPs had characteristics of gld homozygotes, demonstrating close linkage between these genes. The identification of an RFLP closely linked to the gld gene provides a starting point for the identification of a genetic defect that results in abnormal T cells and autoimmune disease.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.167.2.688
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1988
    detail.hit.zdb_id: 1477240-1
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